Itch

Physiological background

Itch results from activation of specialized afferent unmyelinated C fibers in the skin. These fibers are anatomically identical to those that conduct pain but differ in function and stimulus transmission to the brain. They contain a number of receptors such as histamine receptors, PAR-2, endothelin receptor, and TRPV1, and mediators such as histamine, tryptase, endothelin, interleukins, substance P, bradykinin, and prostaglandins are involved in triggering and amplification. These are released from mast cells, among others. Like pain, itch can be triggered peripherally or centrally.

Symptoms

Itching is defined as an unpleasant sensory sensation that triggers the desire to scratch. Associated symptoms such as burning, pain, or stinging may occur.

Causes

Skin disorders:

  • Dry skin, eczema, desiccation eczema.
  • Atopic dermatitis (neurodermatitis)
  • Psoriasis
  • Infectious diseases such as scabies, lice and other parasitic infections, fungal infections, chickenpox, bath dermatitis.
  • Allergy, hives
  • Insect bites, mosquito bites
  • Prurigo nodularis, lichen planus
  • Burns

Systemic diseases:

  • Diabetes mellitus, thyroid disease, gout.
  • Renal insufficiency, uremia
  • Neurogenic itching, e.g., cholestasis.
  • Neuropathic itch due to impairment and damage of nerve pathways: postzoster neuralgia, multiple sclerosis, brain tumors.
  • HIV
  • Tumors
  • Blood diseases such as leukemia, lymphoma

Drugs and substances:

Other causes:

  • Pregnancy
  • Psychogenic pruritus, e.g., due to delusions (parasitophobia, dermatozoa delusion).
  • Psychological causes
  • Idiopathic pruritus with no apparent cause
  • Age: dry skin, increased sensitivity to histamine.

Monitoring

Because itching is an individual sensory sensation, a visual analog scale (VAS) is used to “measure” it, as with pain. The patient marks the severity of the itch on a scale of 1-10, allowing the progression of symptoms and the success of treatment to be tracked. An itch diary is also helpful.

Complications

  • Scratching and rubbing can lead to skin damage, peeling, scarring, worsening of symptoms, and bacterial superinfection, among other complications. In addition, a vicious cycle can occur when scratching exacerbates itching, such as in atopic dermatitis. An additional problem is scratching at night during sleep (in atopic dermatitis up to 20% of sleep!).
  • Sleep disturbances
  • Impairment of quality of life and mental health.
  • Sensitization with severe itching skin (light touch, clothing).

Non-drug measures

“Pain inhibits itch” (Yosipovitch et al., 2003) Inflicting pain is well effective against itch and results in pleasantly experienced relief:

  • Mechanical stimuli such as scratching, rubbing, slapping. However, scratching may contribute to a substantial worsening of itching. Adverse effects: see complications.
  • Cold: cold water, ice, cold hot pack.
  • Electrical stimulation with skin electrodes, small electric shocks.

The analgesic μ-opioids can induce and exacerbate itching. μ-Opioid antagonists, on the other hand, are antipruritic. Cooling helps, as itching worsens with increasing heat:

  • Cool environment.
  • Wear light clothing.
  • Take a lukewarm or cool shower.
  • Avoid alcohol and strongly spiced foods.
  • Rub cooling hydrolotions and gels (can be stored in the refrigerator).
  • At night in bed, the discomfort worsens, so provide a cool climate there as well. A cool shower before bedtime can have a positive effect.

Other measures:

  • Cut nails, wear light cotton gloves at night (nocturnal itching!).
  • Distraction to forget about the itch.
  • Avoid drying the skin with soaps.
  • UV irradiation

Causal drug treatment

Whenever possible, the underlying disease should be treated, for example, by treating an infection with anti-infectives.

External drug treatment

Essential oils and their components:

Skin care products:

  • Creams and lotions nourish and protect the affected and dry skin. Hydrolotions have an additional cooling effect and can be applied over large areas.

Antihistamines:

Topical glucocorticoids:

  • Are not primarily antipruritic, but have a secondary effect by inhibiting underlying inflammation. Hydrocortisone is available without a doctor’s prescription. Glucocorticoids are also used internally.

Local anesthetics:

Tannins:

  • Are commonly used, for example, in the treatment of chickenpox.

Zinc oxide:

Capsaicin (TRPV1 agonists):

  • Is antipruritic in concentrations of 0.025 to 0.075%. It must be applied 3-6 times daily. It appears to be well effective but may initially cause worsening of symptoms. Appropriate preparations must be made in a pharmacy, see under capsaicin.

Calcineurin inhibitors:

Internal drug treatment

Antihistamines:

  • Dimetinden maleate, for example. A high dose may be necessary. They are effective only when histamine is causally involved in the disease process, as in urticaria. Antihistamines of the 1st generation are sedating, which can have a positive effect on an agitation and sleep disturbances.

Mast cell stabilizers:

  • Ketotifen can be used for itching due to urticaria of various causes and atopic dermatitis, among others.

Leukotriene antagonists:

  • Montelukast, for example, is reported to be effective for itching caused by aquagenic urticaria. It is not approved for this indication in many countries.

Glucocorticoids:

  • Are also administered internally (see above).

Antidepressants:

Antiepileptic drugs:

  • Such as gabapentin and pregabalin are thought to inhibit conduction of stimuli to the brain. They are used, among other things, in neuropathically triggered itching, such as postzoster neuralgia.

μ-Opioid antagonists:

  • Naloxone and naltrexone, among others, are used to treat pruritus in cholestasis because it results from accumulation of endogenous prurigenous opioids.
  • Methylnaltrexone (local use, not commercially available).
  • κ-Opioids- are also antipruritic